Abstract 3564: ARID1A promotes endocrine resistance in ER+ breast cancer cells.
Bibliographic record
Abstract
Abstract We recently identified the ARID1A gene as a new candidate tumor suppressor gene (TSG), mutated in the T47D cells, an ER+ breast cancer cell line. We have shown previously that re-expression of ARID1A in T47D cells inhibits both proliferation and anchorage-independent growth and also that nuclear expression of ARID1A is progressively decreased during the later stages of breast tumor progression. ARID1A encodes a member of the SWI/SNF family of proteins, which function to ‘remodel’ chromatin and thereby regulate gene expression programs. Most breast cancers express the estrogen receptor (ER), and are thus responsive to the mitogenic effects of the estrogen hormone as well as to the anti-proliferative effects of anti-estrogen therapies. To uncover the potential role of ARID1A in the regulation of estrogen signaling in ER+ breast cancer cells, we tested if re-expression of ARID1A may also affect estrogen-dependent growth. Surprisingly, we found that re-expression of ARID1A in T47D cells results in a decrease in the proliferative response of these cells to estrogen but also to a decrease in the viability of the cells in hormone-depleted conditions. Then, to further investigate if the loss of ARID1A may promote estrogen-independent growth, we silenced ARID1A expression by shRNA in MCF-7 cells that express moderate levels of ARID1A protein. We found that ARID1A-silencing increases the survival of MCF-7 cells in the absence of hormones. In addition, we also observed that phosphorylation of FAK and Src, whose activities have been suggested to be important in endocrine resistance, is highly increased in the absence of ARID1A. All together, these results suggest that loss of ARID1A can promote endocrine-resistance in ER-positive breast cancer cells. Citation Format: Catherine Chabot, Mark Basik. ARID1A promotes endocrine resistance in ER+ breast cancer cells. [abstract]. In: Proceedings of the 104th Annual Meeting of the American Association for Cancer Research; 2013 Apr 6-10; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2013;73(8 Suppl):Abstract nr 3564. doi:10.1158/1538-7445.AM2013-3564
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How this classification was reachedexpand
Full frame machine prediction
Teacher imitationNot calibrated prevalence, not ground truth. Human validation pending. The Gemma side is a direct model label for every work in the frame, read from the title-only record. The Codex side is a classifier learned from the 10,348 direct Codex labels and calibrated to design-weighted sample rates; fields without enough sample support carry no Codex call. Candidate is the union of the two sides; consensus is their intersection. These outputs are machine_predicted_unvalidated and are not human labels.
Distilled classifier scores by category (both heads)
| Category | Codex | Gemma |
|---|---|---|
| Metaresearch | 0.000 | 0.000 |
| Meta-epidemiology (narrow) | 0.000 | 0.000 |
| Meta-epidemiology (broad) | 0.000 | 0.000 |
| Bibliometrics | 0.000 | 0.000 |
| Science and technology studies | 0.000 | 0.000 |
| Scholarly communication | 0.000 | 0.000 |
| Open science | 0.000 | 0.000 |
| Research integrity | 0.000 | 0.001 |
| Insufficient payload (model declined to judge) | 0.004 | 0.002 |
Machine scores (provisional)
The two teacher heads of the student model, read on this work. A score orders the frame for review; it never asserts a category, and the validation status ships verbatim with every row.
Baseline scores from an immature model (maturity gate not passed, 7 training rounds). Scores rank; they never assert a category.
score_only:v0-immature-baseline · verbatim from the scoring run: score_only means the number may rank works, and no category label ships from itClassification
machine, unvalidatedMachine predicted; a candidate call from one source (direct Gemma or distilled Codex), not a consensus.
How this classification was reached, model by model and score by score, is at the end of the page under "How this classification was reached".